STUDY DESIGN: Biomechanical and radiographical study on cadaveric spines. OBJECTIVE: To explain the pathogenesis of vertebral "anterior wedge" deformity, which causes senile kyphosis. SUMMARY OF BACKGROUND DATA: This deformity arises with minimal trauma and is difficult to reproduce in cadaveric spines. We hypothesize that wedging is created by a 2-stage process. First, excessive loading damages a vertebral endplate and decompresses the adjacent intervertebral disc. This alters load sharing between the vertebral body cortex and trabeculae so that subsequent cyclic loading causes progressive collapse of the unsupported anterior cortex. METHODS: Thirty-four cadaveric thoracolumbar "motion segments," aged 70 to 98 years, were positioned in flexion and overloaded in compression. Physiologically reasonable cyclic compressive loading was then applied to each flexed specimen, at progressively higher loads, for up to 2 hours. Before and after initial overload and again after cyclic loading, the distribution of loading on the vertebra was assessed from measurements of compressive stress within the adjacent disc. These "stress profiles" were repeated in the neutral, flexed, and extended postures. Progressive vertebral body deformity was assessed radiographically. RESULTS: Compressive overload induced endplate fracture at an average force of 2.31 kN. There was minimal anterior wedging, but pressure in the adjacent disc nucleus (in flexion) fell by an average of 55% and neural arch load bearing increased by 166%. Subsequent cyclic loading exaggerated these changes and concentrated compressive stress within the anterior annulus. After both stages, height of the anterior and posterior vertebral cortexes was reduced by 32% and 12%, respectively, so that anterior wedging of the vertebral body increased from 5.0° to 11.4° on average. All changes were highly significant (P < 0.001). CONCLUSION: Anterior wedge deformities can be created consistently by a 2-stage process involving initial endplate damage, followed by progressive collapse of the anterior cortex. Detecting initial endplate damage may be important to minimize vertebral deformity in patients with osteoporosis. LEVEL OF EVIDENCE: N/A.
STUDY DESIGN: Biomechanical and radiographical study on cadaveric spines. OBJECTIVE: To explain the pathogenesis of vertebral "anterior wedge" deformity, which causes senile kyphosis. SUMMARY OF BACKGROUND DATA: This deformity arises with minimal trauma and is difficult to reproduce in cadaveric spines. We hypothesize that wedging is created by a 2-stage process. First, excessive loading damages a vertebral endplate and decompresses the adjacent intervertebral disc. This alters load sharing between the vertebral body cortex and trabeculae so that subsequent cyclic loading causes progressive collapse of the unsupported anterior cortex. METHODS: Thirty-four cadaveric thoracolumbar "motion segments," aged 70 to 98 years, were positioned in flexion and overloaded in compression. Physiologically reasonable cyclic compressive loading was then applied to each flexed specimen, at progressively higher loads, for up to 2 hours. Before and after initial overload and again after cyclic loading, the distribution of loading on the vertebra was assessed from measurements of compressive stress within the adjacent disc. These "stress profiles" were repeated in the neutral, flexed, and extended postures. Progressive vertebral body deformity was assessed radiographically. RESULTS: Compressive overload induced endplate fracture at an average force of 2.31 kN. There was minimal anterior wedging, but pressure in the adjacent disc nucleus (in flexion) fell by an average of 55% and neural arch load bearing increased by 166%. Subsequent cyclic loading exaggerated these changes and concentrated compressive stress within the anterior annulus. After both stages, height of the anterior and posterior vertebral cortexes was reduced by 32% and 12%, respectively, so that anterior wedging of the vertebral body increased from 5.0° to 11.4° on average. All changes were highly significant (P < 0.001). CONCLUSION: Anterior wedge deformities can be created consistently by a 2-stage process involving initial endplate damage, followed by progressive collapse of the anterior cortex. Detecting initial endplate damage may be important to minimize vertebral deformity in patients with osteoporosis. LEVEL OF EVIDENCE: N/A.
Authors: MeiLissa McKay; Timothy M Jackman; Amira I Hussein; Ali Guermazi; Jingjiang Liu; Elise F Morgan Journal: Bone Date: 2019-11-06 Impact factor: 4.398
Authors: Annemarijn Weber; Stephanie M D Huysmans; Sander M J van Kuijk; Silvia M A A Evers; Elisabeth M C Jutten; Rachel Senden; Aggie T G Paulus; Joop P W van den Bergh; Rob A de Bie; Johannes M R Merk; Sandrine P G Bours; Mark Hulsbosch; Esther R C Janssen; Inez Curfs; Wouter L W van Hemert; Martijn G M Schotanus; Paul de Baat; Niek C Schepel; Willem A den Boer; Johannes G E Hendriks; Wai-Yan Liu; Marinus de Kleuver; Martin H Pouw; Miranda L van Hooff; Eva Jacobs; Paul C P H Willems Journal: BMJ Open Date: 2022-05-24 Impact factor: 3.006
Authors: Timothy M Jackman; Amira I Hussein; Cameron Curtiss; Paul M Fein; Anderson Camp; Lidia De Barros; Elise F Morgan Journal: J Bone Miner Res Date: 2015-12-24 Impact factor: 6.741
Authors: Eva Jacobs; Rachel Senden; Christopher McCrum; Lodewijk W van Rhijn; Kenneth Meijer; Paul C Willems Journal: Clin Interv Aging Date: 2019-04-11 Impact factor: 4.458